Benign prostatic hypertrophy (BPH) afflicts most men over the age of 55. Little is known about the etiology of the disease, although endocrine imbalance accompanying aging has been implicated. Recent observations on hyperplastic human prostate indicate that during the course of the disease an estrogen gene product (the progesterone receptor) is induced. This observation indicates a possible role of endogenous estrogen in the pathogenesis of BPH. We propose to study the process of enlargement of the prostate by histological and biochemical methods. This includes study of estrogen, progesterone, and androgen receptors; 7 yield hydroxylase activity; stromal protein synthesis; DHT, estrogen, progesterone, and androstandeiol concentrations in prostate tissue; serum testosterone, Tamoxifen, progesterone and estradiol levels. To accomplish this, we will study: 1) "normal" prostate from kidney donors, 2) the effect of treating patients with Tamoxifen, prior to prostate resection, 3) samples taken from trans-uretheral resection patients. These various data will then be correlated with progesterone and estrogen receptor concentrations. Furthermore, we shall purify the progesterone receptor from prostate and prepare antibodies against it. Utilizing the antibodies to the receptor, we shall determine tissue localization, and more adequately measure the receptor.